1. Field of the Invention
This invention relates to a treatment to increase the hatchability of fertile domestic turkey eggs. In particular, the present invention relates to a composition and a method of injecting fertile turkey eggs with exogenous pyridoxine to enhance the hatchability thereof.
2. Description of the Prior Art
The national average hatch rate of turkey eggs is about 20% lower than that of chicken eggs. Many variables contribute to this low hatch record in turkeys, but it is well recognized in the turkey industry that one factor is a deficiency of vitamins in the diet of breeder turkey hens. To cure this deficiency, modern commercial diets are fortified with a variety of synthetic vitamins. However, the relationship between vitamins and hatchability in the turkey remains complex and unresolved. Preliminary investigations have revealed that pyridoxine drops to low levels in the egg with maternal age of the hen [Robel, Fed. Amer. Soc. Exp. Biol. Med. 41: 1129 (1982); Robel, Poult. Sci. 62: 1751-1756 (1983)]. Environmental stress and the presence of vitamin binding proteins may also be factors in pyridoxine deficiency.
Robel [Comp. Biochem. Physiol., B: Comp, Biochem. 84B: 265-267 (1987)] reported that, as a result of certain field stress factors, certain breeder turkey hens experience hormonal imbalance which causes significantly high levels of avidin to be deposited into the albumenous portion of the egg. Avidin, which is a glycoprotein secreted in the magnum region of the oviduct of the hen, is hormonally induced and binds with biotin, rendering the nutrient unavailable for use. During the initial stages of development, the embryos are not adversely affected by the high levels of avidin because the yolk, which is protected by the yolk sac, provides a sufficient supply of free biotin for normal development. Following the second quarter of incubation, approximately 15-16 days of incubation, the yolk sac ruptures, and the avidin-rich albumen passes progressively into the yolk. At this point, a biotin deficiency occurs within the eggs as the high concentration of avidin makes biotin unavailable to the embryo by forming an avidin-biotin complex.
Robel et al. [Poult. Sci. 66: 1429-1430 (1987)] found that by injecting the avidin-rich eggs with exogenous d-biotin in an inert liquid carrier after at least 23 days of incubation, the eggs were replenished with the supply of free biotin necessary for embryonic survival. The result was an increase in hatch rate up to 5%.